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June 19, 2015Journal of Biological ChemistryOpen Access

Absence of the Regulator of G-protein Signaling, RGS4, Predisposes to Atrial Fibrillation and Is Associated with Abnormal Calcium Handling

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Key result

Global genetic deletion of RGS4 in mice predisposed to atrial fibrillation more frequently than in control littermates due to enhanced Gαq/11-IP3 pathway activity and abnormal calcium release.

Why the study?

Does global genetic deletion of RGS4 predispose to atrial fibrillation and abnormal calcium handling in mice?

Population

Mice with global genetic deletion of RGS4 (RGS4) and normal littermate controls (RGS4), including isolated…

Comparison

Global genetic deletion of RGS4 (RGS4(-/-)) vs Normal littermate controls (RGS4(+/+))

Design

Preclinical

Authors

AOAaisha OpelRoyal Brompton & Harefield NHS Foundation TrustMNMuriel NoblesQueen Mary University of LondonDMDavid MontaigneCardiac Imaging

Discussion

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Implication

No change to AF practice; leaves open RGS4 modulation as hypothesis-generating target in humans.

Structured PICO

Does global genetic deletion of RGS4 predispose to atrial fibrillation and abnormal calcium handling in mice?

P
Population
Mice with global genetic deletion of RGS4 (RGS4(-/-)) and normal littermate controls (RGS4(+/+)), including isolated atrial cells and left atria.
I
Intervention
Global genetic deletion of RGS4 (RGS4(-/-))
C
Comparator
Normal littermate controls (RGS4(+/+))
O
Outcome
Development of atrial fibrillation during in vivo electrophysiology using atrial burst pacingsurrogate

The absence of RGS4 predisposes to atrial fibrillation through enhanced Gαq/11-IP3 pathway activity and abnormal calcium handling.

Cite This Study

Opel et al. (2015) studied Atrial fibrillation. Global genetic deletion of RGS4 vs. Normal littermate controls (RGS4(+/+)) was evaluated on Development of atrial fibrillation during in vivo electrophysiology using atrial burst pacing. Global genetic deletion of RGS4 in mice predisposed to atrial fibrillation more frequently than in control littermates due to enhanced Gαq/11-IP3 pathway activity and abnormal calcium release.

synapsesocial.com/papers/6a13069383732aa7db9ec1dchttps://doi.org/10.1074/jbc.m115.666719

Topics

Atrial fibrillationPersistent AF management
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Evidence for enhanced M3 muscarinic receptor function and sensitivity to atrial arrhythmia in the RGS2-deficient mouse2009 · 58 citations
  2. 2Atrial Tachyarrhythmia in Rgs5-Null Mice2012 · 18 citations
  3. 3Cardiac RGS Proteins in Human Heart Failure and Atrial Fibrillation: Focus on RGS42023 · 11 citations
  4. 4Potential Role of Regulator of G‐Protein Signaling 5 in the Protection of Vagal‐Related Bradycardia and Atrial Tachyarrhythmia2016 · 4 citations
  5. 5Dual loss of regulator of G protein signaling 2 and 5 exacerbates ventricular myocyte arrhythmias and disrupts the fine-tuning of Gi/o signaling2022 · 3 citations